Science, Art, Litt, Science based Art & Science Communication
Your Biological Age Can Be Different From Your Actual (Chronological)Age!
Recently I have seen an old lady teasing an young girl who became breathless after climbing up a few steps. "Look I am 78. But still I can climb steps with ease. I can go anywhere I want without any difficulty. I don't have joint pains like you people have. What are you eating? Rubbish! Ha, ha,ha".
To tell you the truth I really got irritated with this ridicule. Because not everybody will be alike and different people will age differently 'biologically'. Yes, what you eat has some effect on your health but that is not the only reason why you 'age sooner than you should be aging actually'.
People age in different ways. Biological age is a metric that scientists use to predict health risks, the relevance of which can be enhanced by combining different markers. Particularly important markers are frailty and the epigenetic clock (4).
In humans, aging represents the accumulation of changes in a human being over time. There are some theories that explain this process. Biological theories of aging in humans fall into two main categories: programmed aging theories and damage theories. The programmed aging theories imply that aging follows a biological timetable, perhaps a continuation of the one that regulates childhood growth and development. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defense responses. The damage theories emphasize environmental assaults to living organisms that induce cumulative damage at various levels as the cause of aging.
Biological age can differ from chronological age, and the idea of measuring biological age is that it can indicate health risks or the risk of early death—and thus hopefully provide new opportunities for preventative healthcare.
From the tap dancing 90-year-old to the 40-year-old who struggles to run a mile, we all know people who seem surprisingly young or old for their age. Scientists think that it may be possible to distinguish between two types of age: biological age, a measure of how well the body functions, and chronological age, your age in years. Epigenetics, the science of how environmental factors influence our genes, is a promising way to understand the link between the two—and aging in general (2).
People grow old at vastly different rates, but the underlying drivers of aging likely remain the same. Ageing begins even before a baby's birth! The level of oxygen the women exposed to during their pregnancy - because of smoking, using old cooking devices, using timber and cow dung cakes for cooking, pollution, living at higher altitudes where oxygen levels will be low - dictate the rate at which their offspring age as adult. A recent study at Duke University, analyzed the health of nearly one thousand 38-year-olds and found that some resembled people a decade older while others appeared years younger. Researchers determined this “biological age” based on health indicators such as body mass index, blood pressure and cholesterol level. The finding tapped into a mystery that has long captivated scientists and the public alike — why some people can live to 120 with no disease, and others are already in bad shape at age 60.
A handful of recent studies have offered some tantalizing clues. Molecular mayhem within cells, scientists suggested this year, may lie at the root of aging. After examining populations of proteins in the brains and livers of rats, Hetzer and colleagues reported in Cell Systems that long-lived brain proteins appear to become damaged over time. “These are proteins involved in essential cellular functions,” Hetzer says. Unlike liver cells, brain cells rely on proteins that can survive for an animal’s lifetime. Some of those proteins help control messages that pass between brain cells, for example, while others help keep the cell organized. The breakdown of these proteins could be a key driver of aging, Hetzer says.
As could the unraveling of cells’ DNA, another study suggested. In healthy young people, long stretches of DNA pack tightly together in neat bundles called heterochromatin. These bundles aren’t packaged quite so well in old people, researchers comparing DNA from the teeth of young and old people found. The researchers originally identified the disorganization of DNA bundles in people with a premature-aging disorder known as Werner syndrome. The change in the 3-D architecture of the genome gives proteins easy access to stretches of DNA that are supposed to be tucked away.
Beyond the deterioration of proteins and DNA packaging, the body may age when essential barriers break down. When young stem cells in the brain divide, they build a wall that sequesters junky proteins into daughter cells. (This junk mucks with cellular machinery, a problem for stem cells churning out new brain cells.) But old stem cells aren’t so tidy, scientists reported this year in Science. Old stem cells in the brain had worn-out walls inside an organelle called the endoplasmic reticulum. These weakened walls let cellular junk seep back in during division, cutting down on the stem cells’ ability to produce new cells.
Another protective wall, the blood-brain barrier, might also waste away with time. Usually this barrier guards the brain from dangerous toxins in the blood. But MRI scans measuring barrier permeability in living human brains found that old people had leaky walls around the hippocampus, a structure involved in learning and memory. Researchers linked the leaky walls to damage to pericytes, cells found within the blood-brain barrier and crucial to its formation.
Differences in barrier integrity also showed up among old people. Those with learning and memory problems had more pericyte damage than healthy individuals of the same age, Berislav Zlokovic of the University of Southern California in Los Angeles and colleagues reported in Neuron. Breakdown of this brain barrier may kick off some of the cognitive troubles of old age, the authors proposed.
All in all, scientists continue to chip away at the mysteries of growing old. The molecular events identified this year add to previously discovered signs of aging — the shortening of telomeres, the protective caps on chromosomes, for example, and damage to mitochondria, the energy factories of cells. But the picture isn’t complete, or simple. Big questions remain, including how to distinguish healthy aging from disease, as well as the roles of genetics versus environment.
How shortening of telomeres cause aging: In humans and other animals, cellular senescence (to grow old) has been attributed to the shortening of telomeres (Telomeres are the caps at the end of each strand of DNA that protect our chromosomes, like the plastic tips at the end of shoelaces) at each cell Division. When telomeres become too short, the cells die. The length of telomeres is therefore the "molecular clock". This agrees with the 'aging-clock theory' which suggests that an aging sequence is built into the operation of the nervous or endocrine system of the body. In rapidly dividing cells, shortening of the telomeres would provide such a clock. This idea is in contradiction with the evolutionary based theory of aging.
When we think of the DNA that makes up our chromosomes, we usually focus on our genes. But at the end of every chromosome in our body lies a long chain of repetitive DNA called a telomere, which acts as a protective cap. As we age, these caps get shorter. Now studies find that chronic pain and phobic anxiety are linked with shorter telomeres, which suggests that sufferers of these ailments may be aging prematurely! Time naturally shortens telomeres because whenever a cell divides, a portion of the telomere is not replicated. But telomere length can be reduced by other stressors, too, including depression, trauma andobesity. A recent Harvard University study adds anxiety to the list. People with high phobic anxiety, such as that characteristic of panic disorder and agoraphobia, had shorter telomeres, according to a paper published in PLOS ONE.
Telomeres have experimentally been shown to shorten with each successive cell division. Shortened telomeres activate a mechanism that prevents further cell multiplication. This may be particularly limiting to tissues such as bone marrow and the arterial lining where cell division occurs repeatedly throughout life. The quantity of the hematopoietic stem cells that produce the blood components residing in the bone marrow of human beings have been found to decline with aging. Stem cells regenerative capacity is affected by the age of the recipient. Importantly though, mice lacking telomerase enzyme do not show a dramatically reduced lifespan, invalidating at least simple versions of the telomere theory of aging. Laboratory mice may be an exception for the theory, as they have long hypervariable telomeres, which prolong the period after which telomere shortening would affect life-span. However, wild mouse strains do not, and telomere length in these breeds is unrelated to lifespan.
Shortened telomeres have been observed in several types of cancer, coronary heart disease, hypertension, diabetes and arthritis. Accelerated telomere shortening can signal vulnerability to disease, premature aging or even death. In addition, participants with shorter telomeres had increased pain sensitivity and decreased gray matter volume in pain-processing areas of the brain. Fibromyalgia patients with high levels of both depression and pain had telomeres that looked approximately six years older than those of patients who had lower levels of depression and pain.
Researchers are also finding that your mental patterns and thoughts could be harming your telomeres — essential parts of the cell’s DNA — and affecting your life and health(1). People who score high on measures of cynical hostility have shorter telomeres. When you ruminate, stress sticks around in the body long after the reason for the stress is over. Another culprit is thought suppression, the attempt to push away unwanted thoughts and feelings. Ironic error may also be harmful to telomeres. If we try to manage stressful thoughts by sinking the bad thoughts into the deepest waters of our subconscious, it can backfire. The chronically stressed brain’s resources are already taxed — we call this cognitive load — making it even harder to successfully suppress thoughts. Instead of less stress, we get more. In a small study, greater avoidance of negative feelings and thoughts was associated with shorter telomeres.
Different organs in the same individual too can age differently. For instance, some stem cells vital to lung cell oxygenation undergo premature aging — and stop dividing and proliferating — when their telomeres are defective. The stem cells are those in the alveoli, the tiny air exchange sacs where blood takes up oxygen. In studies of these isolated stem cells and in mice, Armanios’ team discovered that dormant or senescent stem cells send out signals that recruit immune molecules to the lungs and cause the severe inflammation that is also a hallmark of emphysema and related lung diseases.
Another internal process experts use to define human’s biological age is methylation of DNA. As the journal Nature defined, methylation “is a common epigenetic signaling tool that cells use to lock genes in the ‘off’ position.” Researchers added the active role of methylation is unknown, “but it appears that proper DNA methylation is essential for cell differentiation and embryonic development.” This explains how cells that are coded the same — see heart and brain cells — can function differently. If every cell in the human body contains the same DNA sequence, how does a heart cell differ from a brain cell? The answer lies within epigenomics.
The study of epigenomics is the study of a cell’s changes in genetic material. A combined set of these changes are known as an epigenome and they alter cell expression, not DNA sequence. So you don’t have to change the DNA itself in order to change how cells are expressed.
An epigenome is what ensures a heart cell is different from a brain cell in spite of the fact they’re coded the same; it’s as flexible as it is complex. Leading science journal Nature (that is behind the video below) reported a much talked about change stems from DNA methylation. This occurs when a chemical is added to DNA and primes the gene to turn off. Aging accounts for cell change, too. For example, Nature reported an increase in methylation in older brains. Varied eating, smoking, and exercise habits have also been found to influence cells. And a disease like cancer can cause cells to "replicate out of control."
DNA methylation is a mechanism used by cells to control gene expression—whether (and when) a gene is turned on or off. This differs across cells and tissues and has been shown to change gradually as we age. The level of methylation can therefore help determine tissue age.
By charting how age affects DNA methylation levels throughout life, scientists have created an epigenetic clock. This is a widely used method for determining biological age from a DNA methylation sample based on hundreds of epigenetic markers. But new research, published in Genome Biology, suggests the method isn't as reliable as previously thought (2).
The most commonly used version of the clock was originally developed from a large collection of data taken from a range of different tissue types.
Where tissue samples come from anonymous donors, the epigenetic clock allows researchers to estimate their chronological age, give or take a few years. By focusing on biological age, it's been proposed that the epigenetic clock reflects our "true" cellular age. This may be altered by our health or the environment we live in.
Many studies have explored age acceleration—how our clocks might be sped up by illness or the environment, and even how this might relate to the risk of death. In essence, this calculates the difference between chronological and biological age for a set of people. You then take this difference and test whether it correlates with the profile of people suffering from a certain disease.
This possibly allows researchers to look at developmental changes, cumulative environmental effects and cellular aging. But there has also been hype surrounding it.
It's important to remember that there's no evidence that the DNA methylation changes used in the epigenetic clock are anything more than a by-product of aging. In fact, they may not determine our aging.
The original samples used in developing the clock model were predominantly taken from younger people and didn't include many from elderly people. Given what we already know about the biological changes that take place as we age, we wanted to test the clock's accuracy, particularly at the older end of the age spectrum.
Age acceleration studies must take account of this, otherwise they risk being fooled by any age-related phenomenon looking like it is associated with DNA methylation.
By looking at data on elderly people from two large studies, one performed in about 90 elderly postmortem brains and the other in bloods from nearly 1,200 people of all ages, we could compare two epigenetic clock models against our DNA methylation results.
Our analysis of the performance of the clock shows that epigenetic age doesn't move at a steady pace throughout life, and that it performs differently in different tissues. Instead, the clock slows as we age, particularly as we enter old age.
We found clear evidence that the ages of people were systematically underestimated by the epigenetic clock, once people were over the age of about 60. At the moment, we don't know why DNA methylation change slows down in this way, or what mechanisms are behind it.
We already knew that DNA methylation changes are not linear over the lifespan. The clock has been updated to account for the big changes taking place in childhood and adolescence, for example. With the amount of data now available, more detailed and accurate clocks for specific tissues and age ranges are possible.
The epigenetic clock is a useful tool for researchers, but given the limited nature of the DNA methylation profile that the clock is based on, taking it at face value could lead to misleading results(3).
Genetic ties to lifespan: A variation in the gene FOXO3A is known to have a positive effect on the life expectancy of humans, and is found much more often in people living to 100 and beyond - moreover, this appears to be true worldwide. FOXO3A acts on the sirtuin family of genes which have also been shown to have a significant effect on lifespan, in yeast and in nematodes (round worms). Over-expression of the RAS2 gene increases lifespan in yeast by 30%.
How calorie intake effects aging: Diet (specifically, caloric restriction) has been shown to substantially affect lifespan in many animals, including the delay or prevention of many age-related diseases. Typically, this involves caloric intake of 60–70% of what an ad libitum ( refer to the "free-feeding" weight of an animal, as opposed, for example, to the weight after a restricted diet) animal would consume, while still maintaining proper nutrient intake.
Some studies have shown that highly reactive free radicals ( Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can be formed when oxygen interacts with certain molecules. Once formed these radicals can start a chain reaction, like dominoes. Generally, free radicals attack the nearest stable molecule, "stealing" its electron. When the "attacked" molecule loses its electron, it becomes a free radical itself, beginning a chain reaction. Once the process is started, it can cascade, finally resulting in the disruption of a living cell) arise normally during metabolism. Sometimes the body's immune system's cells purposefully create them to neutralize viruses and bacteria. However, environmental factors such as pollution, radiation, cigarette smoke and herbicides can also spawn free radicals.
Normally, the body can handle free radicals, but if antioxidants are unavailable, or if the free-radical production becomes excessive, damage can occur. Of particular importance is that free radical damage accumulates with age. The biological theory of aging that points to a buildup in cells of waste products that presumably interfere with metabolism. Evidence supporting this theory is the presence of a waste product called lipofuscin leading to age pigment. Lipofuscin is formed by a complex reaction that binds fat in the cells to proteins. This waste accumulates in the cells as small granules and increases in size as a person ages.
This damage to cells can be restricted through less metabolic processes through dieting. That is where low calorie intake helps.
Inflammation is your immune system's reaction to irritation, injury, or infection. It's a normal response (and actually a good thing) and it's a natural part of healing. But, it's possible that chronic inflammation could have a negative impact on your body and your health.
Inflammation is the body's attempt at self-protection; the aim being to remove harmful stimuli, including damaged cells, irritants, or pathogens - and begin the healing process. The Role of Inflammation in Age-Related Disease and also in the biological aging process is well documented. For many, inflammation is simply understood as a trajectory of biomarkers, for example the appearance of IL-6 or C-reactive protein (CRP), associated with a disease. However, inflammation is a very complex response to an injury, infection, or other stimulus, in which many different cells types and secreted factors orchestrate protective immunity, tissue repair, and resolution of tissue damage. Whereas acute inflammation limits tissue damage and resolves, chronic prolongation of the inflammatory state leads to progressive tissue damage. The mild pro-inflammatory state of aging is dangerous. Among the causal pathways linked to the major diseases associated with aging, including physical frailty, are changes in body composition, energy imbalance, homeostatic dysregulation, and neurodegeneration. Chronic inflammation is strongly connected with each of these aging phenotypes. Inflammation blocks critical metabolic signals that support muscle maintenance. Skeletal and muscle working conditions, degeneration and regeneration of damaged tissues are determined by inflammation. This in turn causes slow walking and low cognitive speeds.
mTOR, a protein that inhibits autophagy ( the natural, destructive mechanism that disassembles, through a regulated process, unnecessary or dysfunctional cellular components) has been linked to ageing through the insulin signalling pathway. It has been found, in various model species, that caloric restriction leads to longer lifespans, an effect that is likely mediated by the nutrient-sensing function of the mTOR pathway. mTOR functions through nutrient and growth cues leading scientists to believe that dietary restriction and mTOR are related in terms of longevity. When organisms restrict their diet, mTOR activity is reduced, which allows an increased level of autophagy. This recycles old or damaged cell parts, which increases longevity and decreases the chances of being obese. This is thought to prevent spikes of glucose concentration in the blood, leading to reduced insulin signalling. This has been linked to less mTOR activation as well. Therefore, longevity has been connected to caloric restriction and insulin sensitivity inhibiting mTOR, which in turns allows autophagy to occur more frequently. It may be that mTOR inhibition and autophagy reduce the effects of reactive oxygen species (chemically reactive molecules containing oxygen) on the body, which damage DNA and other organic material, so longevity would be increased.
Life-span is selected. Traits that benefit early survival and reproduction will be selected for even if they contribute to an earlier death. Such a genetic effect is called the antagonistic pleiotropy (the phenomenon where one gene controls for more than one phenotypic trait in an organism. Antagonistic pleiotropy is when one gene controls for more than one trait where at least one of these traits is beneficial to the organism's fitness and at least one is detrimental to the organism's fitness) effect when referring to a gene (pleiotropy signifying the gene has a double function - enabling reproduction at a young age but costing the organism life expectancy in old age) and is called the disposable soma ( presumes that the body must budget the amount of energy available to it) effect when referring to an entire genetic programme (the organism diverting limited resources from maintenance to reproduction). Some of the genetic variants that increase fertility in the young are now known to increase cancer risk in the old. Such genes include p53 and BRCA1. The biological mechanisms which regulate lifespan evolved several hundred million years ago.
According to reproductive cell theory the idea that aging is regulated by reproductive hormones that act in an antagonistic pleiotropic manner via cell cycle signalling, promoting growth and development early in life to achieve reproduction, but later in life, in a futile attempt to maintain reproduction, become dysregulated and lead cells to aging.
Autoimmune theory says that the idea that ageing results from an increase in autoantibodies {an antibody (a type of protein) produced by the immune system that is directed against one or more of the individual's own proteins} that attack the body's tissues. A number of diseases associated with aging are autoimmune in this way. While inflammation is very much evident in old mammals, even severe combined immunodeficiency, SCID ( a genetic disorder characterized by the disturbed development of functional T cells and B cells of the immune system caused by numerous genetic mutations that result in heterogeneous clinical presentations) mice in SPF colonies still experience senescence ( getting old).
Genetic damage has two types. Mutations are damages to the DNA sequence, while epimutation is damage to the DNA scaffolding which regulates gene expression in the cell. Both ultimately harm our health by causing abnormal gene expression. Some (epi-)mutations lead to cancers, which are the uncontrolled growth and division of cells.
Gene loss theory of ageing: It has been established that humans lose approximately 0.6% of the DNA in their heart muscle cells annually. Yearly DNA loss in the brain and lymphocytes also happens with such a percentage. This is almost certainly (or probably the) central cause of aging.
Moreover, ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code. As we age, more and more errors accumulate in the code because of the division of cells throughout our lives. Misrepairs that cannot correct the errors lead to damage of cells.
Premature aging is a consequence of mis-construction of tissues and organs during development, which is caused by genetic disorders. The abnormality of tissue structure is the common point between premature aging and normal aging, and it links a defective development and a defective repair.
A person's biological age is a better measure for determining a person's health than is chronological age. The former is more closely tied to one's risk of age-related diseases, such as dementia and osteoporosis, than was one's chronological age. Therefore, all the 20year old people are not the same and so are all 60 or 100 year old human beings.
Next time you blame somebody for his or her general health think of all these factors to determine their biological age and try to understand how their bodies are operating and coping with all these factors! And please don't ridicule people for what they are and things that are not in their control.
And need I add - taking only chronological age into consideration while issuing insurance policies and selecting candidates for jobs is out of date now?
Citations:
1. http://ideas.ted.com/could-your-thoughts-make-you-age-faster/
2. https://sciencex.com/news/2020-01-aging-epigenetic-clocks-older.htm...
3. Louis Y. El Khoury et al. Systematic underestimation of the epigenetic clock and age acceleration in older subjects, Genome Biology (2019). DOI: 10.1186/s13059-019-1810-4
4. https://medicalxpress.com/news/2020-02-biological-age-health.html?u...
Updates:
Difference between retina's biological age and person's real age linked to heightened death risk
The difference between the biological age of the retina, the light sensitive layers of nerve tissue at the back of the eye, and a person's real (chronological) age, is linked to their risk of death, finds research published online in the British Journal of Ophthalmology.
This 'retinal age gap' could be used as a screening tool, suggest the researchers.
A growing body of evidence suggests that the network of small vessels (microvasculature) in the retina might be a reliable indicator of the overall health of the body's circulatory system and the brain.
While the risks of illness and death increase with age, it's clear that these risks vary considerably among people of the same age, implying that 'biological aging' is unique to the individual and may be a better indicator of current and future health, say the researchers.
Several tissue, cell, chemical, and imaging-based indicators have been developed to pick up biological aging that is out of step with chronological aging. But these techniques are fraught with ethical/privacy issues as well as often being invasive, expensive, and time consuming, say the researchers.
They therefore turned to deep learning to see if it might accurately predict a person's retinal age from images of the fundus, the internal back surface of the eye, and to see whether any difference between this and a person's real age, referred to as the 'retinal age gap', might be linked to a heightened risk of death.
Deep learning is a type of machine learning and artificial intelligence (AI) that imitates the way people acquire certain types of knowledge. But unlike classic machine learning algorithms that are linear, deep learning algorithms are stacked in a hierarchy of increasing complexity.
The researchers drew on 80,169 fundus images taken from 46,969 adults aged 40 to 69, all of whom were part of the UK Biobank, a large, population-based study of more than half a million middle aged and older UK residents.
Some 19,200 fundus images from the right eyes of 11,052 participants in relatively good health at the initial Biobank health check were used to validate the accuracy of the deep learning model for retinal age prediction.
This showed a strong association between predicted retinal age and real age, with an overall accuracy to within 3.5 years.
The retinal age gap was then assessed in the remaining 35,917 participants during an average monitoring period of 11 years.
During this time, 1871(5%) participants died: 321(17%) of cardiovascular disease; 1018 (54.5%) of cancer; and 532 (28.5%) of other causes including dementia. The proportions of 'fast agers'—those whose retinas looked older than their real age– with retinal age gaps of more than 3, 5, and 10 years were, respectively, 51%, 28%, and 4.5%. Large retinal age gaps in years were significantly associated with 49%-67% higher risks of death, other than from cardiovascular disease or cancer. And each 1 year increase in the retinal age gap was associated with a 2% increase in the risk of death from any cause and a 3% increase in the risk of death from a specific cause other than cardiovascular disease and cancer, after accounting for potentially influential factors, such as high blood pressure, weight (BMI), lifestyle, and ethnicity. The same process applied to the left eyes produced similar results. This is an observational study, and as such, can't establish cause. The researchers also acknowledge that the retinal images were captured at one moment in time, and that the participants may not be representative of the UK population as a whole. Nevertheless, they write: "Our novel findings have determined that the retinal age gap is an independent predictor of increased mortality risk, especially of non-[cardiovascular disease]/ non-cancer mortality. These findings suggest that retinal age may be a clinically significant biomarker of aging." They add: "The retina offers a unique, accessible 'window' to evaluate underlying pathological processes of systemic vascular and neurological diseases that are associated with increased risks of mortality. "This hypothesis is supported by previous studies, which have suggested that retinal imaging contains information about cardiovascular risk factors, chronic kidney diseases, and systemic biomarkers." The new findings, combined with previous research, add weight to "the hypothesis that the retina plays an important role in the aging process and is sensitive to the cumulative damages of aging which increase the mortality risk," they explain. |
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An international team of scientists has for the first time shown that mitochondria, the batteries of the cells, are essential for ageing.
In a study, published today in the EMBO Journal and led by Dr João Passos at Newcastle University, they found that when mitochondria were eliminated from ageing cells they became much more similar to younger cells. This experiment was able for the first time to conclusively prove that mitochondria are major triggers of cell ageing.
This brings scientists a step closer to developing therapies to counteract the ageing of cells, by targeting mitochondria.
Defying ageing in the cell
As we grow old, cells in our bodies accumulate different types of damage and have increased inflammation, factors which are thought to contribute to the ageing process.
The team carried out a series of genetic experiments involving human cells grown in the laboratory and succeeded in eliminating the majority, if not all, the mitochondria from ageing cells. Cells can normally eliminate mitochondria which are faulty by a process called mitophagy. The scientists were able to "trick" the cells into inducing this process in a grand scale, until all the mitochondria within the cells were physically removed.
To their surprise, they observed that the ageing cells, after losing their mitochondria, showed characteristics similar to younger cells, that is they became rejuvenated. The levels of inflammatory molecules, oxygen free radicals and expression of genes which are among the makers of cellular ageing dropped to the level that would be expected in younger cells.
New thinking on mitochondria
Dr João Passos of the Institute for Ageing said: "This is a very exciting and surprising discovery. We already had some clues that mitochondria played a role in the ageing of cells, but scientists around the world have struggled to understand exactly how and to what extent these were involved.
"These new findings highlight that mitochondria are actually essential to the ageing of cells."
The team led by Newcastle University and involving other universities in the UK and the US, also deciphered a new mechanism by which mitochondria contribute to ageing. They identified that as cells grow old, mitochondrial biogenesis, the complex process by which mitochondria replicate themselves, is a major driver of cellular ageing.
"This is the first time that a study demonstrates that mitochondria are necessary for cellular ageing," said Dr Clara Correia-Melo of the Newcastle University Institute for Ageing and the lead author of the study. "Now we are a step closer to devising therapies which target mitochondria to counteract the ageing of cells."
http://www.eurekalert.org/pub_releases/2016-02/nu-mst020316.php
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How old we look is not just about counting the wrinkles at the corners of our eyes or the sunspots that dapple our skin. Scientists may have discovered the first gene responsible for how young—or old—we look to others.
New genome-sequencing research suggests white European people with two copies of variant forms of MC1R, a gene linked to pale skin and red hair, have faces that appear up to two years older than those who are the same age but don’t have both copies. Having only one variant copy of the gene gives people the appearance of looking about one year older on average, the team of Dutch and British researchers concluded. The scientists also discovered that this new genetic association held true even after accounting for factors like wrinkling, reported sun exposure and varied skin tone (pale versus olive).
Of course, even genetic instructions have their limits.
Genetic Secrets to Youthful Looks Revealed
The gene linked to pale skin and red hair appears to have another big role in appearance
http://www.scientificamerican.com/article/genetic-secrets-to-youthf...
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The Emerging View of Aging as a Reversible Epigenetic Process.
https://www.ncbi.nlm.nih.gov/pubmed/28538216
https://www.statnews.com/2020/02/19/biological-aging-steps-consensu...
We need to take steps toward building a consensus definition of biological aging
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http://www.cdc.gov/vitalsigns/cardiovasculardisease/heartage.html
My heart's age is 10 years younger than my actual age!
You can check yours by clicking on the link above
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Pluripotency Factor Actually A Telomere Enlongator
Zscan4, originally believed to be involved in pluripotency of stem cells, is actually triggered by shortened telomeres to regenerate the telomere length. Asian Scientist Newsroom | March 28, 2016 | In the Lab AsianScientist (Mar. 28, 2016) - Scientists from the RIKEN Center for Developmental Biology in Japan, have discovered that the Zscan4 protein is actually a repair mechanism triggered by the shortening of telomeres that takes place during cell division. Zscan4 was originally believed to be involved in the development of pluripotency in stem cells. Their work was published in Stem Cell Reports. Zscan4, a protein that binds to DNA, has posed a mystery for the past decade. It is expressed in mouse embryos at a very specific point of time—the two-cell stage—but is also expressed in embryonic stem cells, but only transiently, so that it is on in about five percent of a given population at a given time. The researchers wondered why the protein was expressed in these specific situations. To address this, they grew a population of mouse embryonic stem cells in culture and took snapshots of the cells at 60-minute intervals for an extended period, seeking clues for what might cause the transient expression of Zscan4. Their initial working hypothesis was that Zscan4 is involved in the maintenance of pluripotency, so they looked its correlation with expression of the Rex1 gene, which is known as a marker of pluripotency. “Unexpectedly, we found that there was no correlation between the two,” says Dr. Yoko Nakai-Futatsugi, the first author of the study. “Instead, we were surprised to find that the stem cells have different cell cycle lengths, and that intriguingly, the expression of Zscan4 is linked to the length of the cell cycle. It tends to be expressed in cells with longer cell cycles.” From this finding and considering the 2010 research showing that Zscan4 is involved in telomere elongations, the researchers speculated that the longer cell cycles may be caused by a process triggered by Zscan4 to lengthen the telomeres. They also found that once cells had expressed Zscan4, in the next generation they had shorter cell cycles, adding weight to the hypothesis that the cells slow their cycle in order to allow the recovery of telomeres, and then speed it up again when the repair is completed. Furthermore, cells with longer cell cycles did in fact have shorter telomeres. In a final test, they engineered stem cells that had a deficiency in Zscan4 expression and, in accordance with the hypothesis, those cells failed to recover from the longer cell cycles and had a higher chance of undergoing cell death. The authors feel these findings could help to ensure the safety of induced pluripotent stem cells, which are currently moving into clinical use. The work has helped them gain a new understanding of the function of Zscan4 and how pluripotent cells work to maintain their ability to replicate in the face of telomere shortening. An interesting remaining question, they explain, is the relationship between Zscan4 and telomerase, an enzyme also involved in telomere repair. They speculate that they are responding to different causes of telomere shortening, and plan to continue work to elucidate this. They are also interested in the question of why Zscan4 is expressed in vivo at the single point of the two-cell stage. It might be, they feel, that it is helping the cells recover from the process of meiosis that the cells undergo before reproduction. The article can be found at: Nakai-Futatsugi and Niwa (2016) Zscan4 Is Activated after Telomere Shortening in Mouse Embryonic Stem Cells.
http://www.cell.com/stem-cell-reports/abstract/S2213-6711(16)00061-8?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2213671116000618%3Fshowall%3Dtrue
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Research into aging requires patience, but a small cadre of scientists is angling to speed up answers by developing the flamboyant, short-lived turquoise killifish as a new mode
http://www.scientificamerican.com/article/live-fast-die-young/?WT.m...
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Could your thoughts make you age faster?
http://ideas.ted.com/could-your-thoughts-make-you-age-faster/
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Does Our Blood Hold the Secrets of Our Longevity?
Your blood reveals a lot of of secrets about your actual age and longevity ...
Are you as old as you feel, as old as you look or as old as your birth certificate says? The best answer may be “none of the above.” Actually, you may be as biologically old as your blood says you are.
For many years, aging researchers have sought markers of biological age, or biomarkers — simple signals that reveal the expected length of your future health. The expected length of future health, after all, is the key biological difference between younger and older people.
Some people have called such markers “biological clocks.” I don’t know about you, but I don’t typically calculate my age by thinking of clocks. I think of calendars. So, I prefer to call these hypothetical signals “biological calendars.”
The importance of these calendars is that they potentially allow researchers to quickly see whether a new drug, diet or other treatment that purports to slow, or even possibly reverse, aging is actually doing so.
Biological calendars of aging can also provide rapid feedback on how a lifestyle change, such as in diet or exercise habits, is affecting your biological age. This insight can motivate people to stick with that change.
https://www.nextavenue.org/blood-hold-secrets-longevity/?__cf_chl_c...
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You bring up an important point. I’ve alluded to much the same thing when I point out that telomere shortening isn’t the only cause of organ atrophy or age-related senescence. At least four types of cells are non-mitotic and therefore don’t undergo this mitosis-related telomere shortening—skeletal muscle, cardiac muscle, neurons, and adipocytes—but they degenerate and die off in old age anyway (at least the first three; I’m less sure of senescence in adipocytes). Presumably their telomeres at age 80–90 are no shorter than they were at age 15–20. They degenerate for other reasons (oxidative damage, protein cross-linking, defective protein folding, mutations affecting gene expression, etc.).--A comparison of nine different approaches over a period of 20 years reveals the most promising indicators for biological age.--Scientists discover new clue behind age-related diseases and food spoilage
https://phys.org/news/2020-02-scientists-clue-age-related-diseases-...
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Researchers discover a new way to fight the aging process and cancer development
lin-52 mutant worms retained motility upon DNA damage induction. lin-52(n771) and WT day 1 adult worms were irradiated or mock-treated with UV-B and their motility was measured after 72 h. Maximum speed per individual is presented (mean +/− SD in red). Two-tailed Mann-Whitney test was used. From left to right, n = 20, 23, 29, 32. Credit: Nature Structural & Molecular Biology (2023). DOI: 10.1038/s41594-023-00942-8
A protein complex prevents the repair of genome damage in human cells, in mice and in the nematode Caenorhabditis elegans, a team of researchers at the University of Cologne has discovered. They also successfully inhibited this complex for the first time using a pharmaceutical agent.
"When we suppress the so-called DREAM complex in body cells, various repair mechanisms kick in, making these cells extremely resilient towards all kinds of DNA damage," said Professor Dr. Björn Schumacher, Director of the Institute for Genome Stability in Aging and Disease at the University of Cologne's CECAD Cluster of Excellence in Aging Research.
Because it contains all of our genetic information, our DNA must be well protected. However, it constantly faces damage caused by environmental influences—or our normal metabolism. Hence, DNA repair is essential for the stability of our genome and the functioning of our cells.
"Our findings for the first time allow us to improve DNA repair in body cells and to target the causes of aging and cancer development," Schumacher added. Still, more research is needed until these results can be translated into new therapies for human patients. The study 'The DREAM complex functions as conserved master regulator of somatic DNA repair capacities' has appeared in Nature Structural & Molecular Biology.
DNA damage leads to aging and disease
Our genetic material is passed on from generation to generation. That is why it is particularly well protected in our germ cells. Highly precise DNA repair mechanisms are at work there, ensuring that only very few changes in the genetic material are passed on to offspring. Thanks to DNA repair, our human genome has been passed on to us by our ancestors for two hundred thousand years. It has always ensured that the genetic information is preserved. DNA is also constantly repaired in our body cells, but only for the duration of the individual's life.
Sometimes, children are born with faulty DNA repair systems, making them age more quickly and develop typical age-related diseases such as neuro-degradation and arteriosclerosis already in childhood. In some cases, they also have an extremely increased risk of cancer. These are all consequences of DNA damage not being properly repaired.
The DREAM complex prevents repairs
Schumacher and his team explored why body cells do not have the same repair mechanisms as germ cells. In experiments with the nematode C. elegans, they found out that the DREAM protein complex limits the quantity of DNA repair mechanisms in body cells: the complex attaches to the DNA's construction plans containing instructions for the repair mechanisms. This prevents them from being produced in large quantities.
Germ cells, however, do not have the DREAM complex. Hence, they naturally produce large quantities of DNA repair mechanisms.
Mammals also have a DREAM complex
In further experiments with human cells in the laboratory (cell culture), the scientists showed that the DREAM complex functions in the same way in human cells. They were also able to override the DREAM complex with a pharmaceutical agent.
"We were very pleased to see the same effect as we did in C. elegans. The human cells were much more resilient towards DNA damage after treatment," said Arturo Bujarrabal, a postdoc in Schumacher's team and lead author of the study. Treatment with the DREAM complex inhibitor also showed amazing effects in mice: The DNA in the retina of mice could be repaired and the function of the eye preserved.
The test was carried out in mice that, like some patients, age prematurely and show a typical degeneration of the eye's retina.
Genome damage also plays a major role in manned spaceflight because of the extremely high radiation in space. A longer stay in space without improved DNA repair is hardly imaginable. Schumacher says, "Therapies that target and improve this newly discovered master regulator of DNA repair could reduce the risk of cancer because genes remain intact."
In addition, the risk of age-related diseases would be reduced because cells can only fulfill their function with an intact genome.
More information: Björn Schumacher, The DREAM complex functions as conserved master regulator of somatic DNA-repair capacities, Nature Structural & Molecular Biology (2023). DOI: 10.1038/s41594-023-00942-8. www.nature.com/articles/s41594-023-00942-8
Journal information: Nature Structural & Molecular Biology
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Scientists can now predict your biological age from pictures of your body
Did you know that your body can age at a different pace to how many birthdays you’ve celebrated? Well, scientists in China have now worked out a new way to measure this ‘biological age’, and it could help to speed up anti-ageing treatments.
The new approach involves the analysis of 3D images of your body parts using artificial intelligence. Specifically, images of your face, tongue, and retina (the layer of cells at the back of your eye that converts light into signals for your brain).
While chronological age represents the number of years you have been alive, your biological age represents how worn the cells in your body are. This rate will vary for different people, meaning that, for many of us, our biological and chronological ages are different.
Usually, scientists estimate biological age through ‘epigenetic clocks’. This is generally determined through the study of levels of methylation – or chemical changes – in your DNA. Previously, biological age was calculated mainly through DNA or blood tests, alongside brain scans.
To create an accessible yet accurate prediction of biological age, the scientists built a model that uses AI to combine facial, tongue and retina images. Pictures of the face can indicate skin health, while your tongue reveals how healthy your microbiome is and your retinas can signal the health of your neurological and cardiovascular systems.
“The fact you can [estimate biological age] with photographs of, among other things, people's faces, gives scientific rigour to a common intuition that some people can look older or younger than their age,” longevity expert Andrew Steele, who was not involved in the study.However, as the new research – published in the Proceedings of the National Academy Of Sciences (PNAS) – points out, individual systems measured by photographs alone may not be helpful markers of biological age on their own. But, as the scientists point out, such images still provide some insights, and are cheaper, easier and less invasive than DNA, blood tests or brain scans.
The researchers, from Macau University of Science and Technology and Shanghai Jiaotong University, both in China, first tested the model on 11,223 healthy people.
They then applied it to 2,840 individuals who were suffering from chronic diseases. The model revealed that the biological ages of these individuals were significantly higher than their chronological ages compared to the healthy individuals.
In the future, the tool could become a helpful estimation of the impacts of chronic diseases on ageing, and vice versa.
According to Steele, the next big question is “how these measures of biological age are affected by anti-ageing interventions – whether that's diet and exercise, or a new longevity pill."
He added: “If we can assess their effectiveness with photographs, in the future we may be able to speed up clinical trials dramatically by using before-and-after photos to assess whether an anti-ageing therapy works.”
(Dr Andrew Steele is a scientist, writer and presenter. )
https://www.sciencefocus.com/news/new-measurement-biological-age
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A Blood Test Could Reveal Your Biological Age And Predict Disease Risk
A new study from a research team has discovered blood-based markers that can reveal someone's biological age, which could help treat various health problems that can happen as our bodies get older.
We have our actual ages – the number of years we've been alive – and then we have biological ages, which in simple terms is the wear and tear on cells and organs. Knowing this biological age can help work out disease risk, tailor treatments, and help us to better understand the different rates at which our bodies break down.
This is how the two aging processes pan out:
Imagine two people aged 65. One rides a bike to work and goes skiing on the weekends and the other can't even climb a flight of stairs.They have the same chronological age, but very different biological ages.
Why do these two people age differently?To help answer this question, the researchers enlisted the help of 196 elderly adults, split into two groups: one of volunteers aged 75 or older who were designated as healthy agers, and one of volunteers aged 65-75 who were classed as rapid agers.
The healthy agers were able to climb a flight of stairs or walk for 15 minutes without resting, while the rapid agers had to take breaks through each activity. The distinction gave the study team the chance to look at differences between the groups on a molecular level.
In particular, the researchers looked for different metabolites; small molecules left by biological processes in the body. They can be used as evidence for which processes are happening, and how well they're running.
A total of 25 metabolites were identified that showed significant differences between the healthy agers and the rapid agers. This group of molecules has been named the Healthy Aging Metabolic (HAM) Index. The team also identified three metabolites that seemed to be particularly important in driving biological aging.
Researchers chose to look at metabolites because they are dynamic. They change in real time to reflect our current health and how we feel, and we have the power to influence them through our lifestyles, diet and environment.
In tests on a separate group, the HAM Index proved to be 68 percent accurate at working out biological age. With more research, it might be possible to develop a blood test for quick and easy biological age assessment.That test could then be run on people at earlier ages, when changes to molecular processes are easier to modify: in someone in their 30s, for example, who is told their biological age is much higher than it should be.
That person could then think about changing aspects of their lifestyle early – whether that's improving their sleep, diet or exercise regime – to hopefully reverse their biological age.
A molecular index for biological age identified from the metabolome and senescence-associated secretome in humans
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Risk factors for faster aging in the brain revealed in new study
In a new study published in Nature Communications, researchers investigated the genetic and modifiable influences on fragile brain regions by looking at the brain scans of 40,000 UK Biobank participants aged over 45.
Previously, the researchers had identified a 'weak spot' in the brain, which is a specific network of higher-order regions that not only develop later during adolescence, but also show earlier degeneration in old age. They showed that this brain network is also particularly vulnerable to schizophrenia and Alzheimer's disease.
In their latest study, the researchers examined 161 risk factors for dementia, and ranked their impact on this vulnerable brain network, over and above the natural effects of age.
They classified these so-called 'modifiable' risk factors—as they can potentially be changed throughout life to reduce the risk of dementia—into 15 broad categories: blood pressure, cholesterol, diabetes, weight, alcohol consumption, smoking, depressive mood, inflammation, pollution, hearing, sleep, socialization, diet, physical activity, and education.
We know that a constellation of brain regions degenerates earlier in aging, and in this new study researchers have shown that these specific parts of the brain are most vulnerable to diabetes, traffic-related air pollution—increasingly a major player in dementia—and alcohol, of all the common risk factors for dementia.
They have found that several variations in the genome influence this brain network, and they are implicated in cardiovascular deaths, schizophrenia, Alzheimer's and Parkinson's diseases, as well as with the two antigens of a little-known blood group, the elusive XG antigen system, which was an entirely new and unexpected finding.
In fact, two of these seven genetic findings are located in this particular region containing the genes of the XG blood group, and that region is highly atypical because it is shared by both X and Y sex chromosomes. This is really quite intriguing as we do not know much about these parts of the genome; our work shows there is benefit in exploring further this genetic terra incognita.
It is with this kind of comprehensive, holistic approach—and once we had taken into account the effects of age and sex—that three emerged as the most harmful: diabetes, air pollution, and alcohol.
This research sheds light on some of the most critical risk factors for dementia, and provides novel information that can contribute to prevention and future strategies for targeted intervention.
The effects of genetic and modifiable risk factors on brain regions vulnerable to ageing and disease, Nature Communications (2024). DOI: 10.1038/s41467-024-46344-2
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High consumption of ultra-processed foods linked to accelerated biological aging
A study conducted by the Research Unit of Epidemiology and Prevention at the I.R.C.C.S. Neuromed in Pozzilli, in collaboration with the LUM University of Casamassima, shows that high consumption of ultra-processed foods is associated with the acceleration of biological aging, regardless of the nutritional quality of the diet. The results were published in the journal The American Journal of Clinical Nutrition.
researchers analyzed data on over 22,000 participants from the Moli-sani Study, one of the largest population cohorts in Europe, and used over thirty different blood biomarkers to measure biological age. Unlike chronological age, which depends exclusively on the date of birth, biological age reflects the biological conditions of our body, including organs, tissues and systems, and can differ from its chronological age.
Using a detailed food frequency questionnaire, researchers were able to estimate participant's consumption of ultra-processed foods, that is foods made in part or entirely with substances not routinely used in the kitchen (e.g., hydrolyzed proteins, maltodextrins, hydrogenated fats), that generally contain various additives, such as dyes, preservatives, antioxidants, anticaking agents, flavor enhancers and sweeteners.
Ultra-processed foods include not only packaged snacks or sugary drinks, but also apparently "harmless" products such as mass-produced or packaged bread, fruit yogurt, some breakfast cereals or meat alternatives, to give a few examples.
The study showed that a high consumption of ultra-processed foods is associated with a significant acceleration of the biological aging of participants. Basically, people turned out to be biologically older than their actual chronological age.
Biological aging is in fact an "internal clock" of our body, which can tick faster or slower than the years marked on the calendar, reflecting the true state of health of the organism.
Their data shows that a high consumption of ultra-processed foods not only has a negative impact on health in general, but could also accelerate aging itself, suggesting a connection that goes beyond the poor nutritional quality of these foods.
Besides being nutritionally inadequate, being rich in sugars, salt and saturated or trans fats, these foods undergo intense industrial processing that actually alters their food matrix, with the consequent loss of nutrients and fiber.
This can have important consequences for a series of physiological functions, including glucose metabolism, and the composition and functionality of the gut microbiota. Also, these products are often wrapped in plastic packaging, thus becoming vehicles of substances toxic to the body.
Simona Esposito et al, Ultra-processed food consumption is associated with the acceleration of biological aging in the Moli-sani Study, The American Journal of Clinical Nutrition (2024). DOI: 10.1016/j.ajcnut.2024.10.006
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Extreme heat makes body clocks tick faster
Exposure to extreme heat could be linked to molecular changes that reflect accelerated ageing. Researchers looked at data from almost 4,000 people and cross-referenced their ‘epigenetic clocks’ — a collection of chemical modifications to DNA as people age — with temperature maps. The team found that people who lived in areas with more hot days had ‘older’ molecular .... However, factors such as how long each person spent outside, and whether they had air conditioning, weren’t taken into account.
https://www.nature.com/articles/d41586-024-04007-8?utm_source=Live+...
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